The Placenta is Simply a Neuroendocrine Parasite

Abstract

This paper will document the early scientific observations that kindled my neuroendocrinological interest in pre‐eclampsia, a life‐threatening disease that affects both mother and baby. My interest in this subject started with the placental origin of melanotrophin activity, moving on, through corticotrophin‐releasing factor and its binding protein, to a tachykinin modified specifically in the placenta by phosphocholine, a post‐translational moiety normally used by parasites to avoid immune surveillance and rejection. This work may finally have led to an understanding of the identity of the elusive placental factor that, whilst attempting to compensate for the poor implantation of the placenta, causes the many symptoms seen in the mother during pre‐eclampsia.

Neurokinin B and pre-eclampsia: a decade of discovery

“…Instead the predominant NKB-like immunoreactivity was found in peaks of much larger molecular mass. A similar observation has also been reported by Lowry [43] who observed that the placental concentrations of processed NKB peptides from normal pregnancies were very low and extracts contained more partially processed material than fully processed products. This was also evident in the maternal blood where NKB precursor peptides could also be found [43].…”

“…A similar observation has also been reported by Lowry [43] who observed that the placental concentrations of processed NKB peptides from normal pregnancies were very low and extracts contained more partially processed material than fully processed products. This was also evident in the maternal blood where NKB precursor peptides could also be found [43]. In contrast the chromatographic profiles from term pre-eclamptic placenta had a single peak that contained significant amounts of processed NKB that corresponded to that of NKB found in the rat brain and to that of synthetic NKB [24,27].…”

Hepatitis E and Acute Liver Failure in Pregnancy

“…The various mechanisms of maternal immune tolerance include: complement inhibition, 59 phosphocholination, 60 upregulation of programmed death ligand-1 over CD4/ CD8 CTLs, 61 alteration of processing and presentation by Major histocompatibility complex, progesterone, 62 shift in Th-1/Th2 cytokine balance, Tregs (regulatory T cells) and placental exosomes. The role of these mechanisms of maternal immune tolerance is still unfolding.…”

Mechanisms of Maternal Immune Tolerance During Pregnancy

“…In these studies, placental neurokinin B and the precursors of corticotropin releasing hormone (CRH), adrenocorticotropin, hemokinin, activin and follistatin were shown to be post-translationally modified by the addition of phosphocholine using a combination of HPLC and two site immunometric analyses. Lowry (Lowry, 2008) suggested that the addition of phosphocholine moieties in placental secreted peptides and proteins may be the rule rather than the exception and that this post translational modification may play an important role in maternal immune tolerance during pregnancy.…”